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- 저자 : Yujiao Zhao (검색결과 3 건)
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Lezhu Su,Lizhou Ou,Yujiao Wen,Yifan Wang,Weilin Zhao,Zhi Zhou,Mei-e Zhong,YONGFA ZHU,Nan Zhou 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.102 No.-
Exploring catalyst materials which are advancing, recyclable and with high catalytic performances toremove persistent organic pollutants such as Quinclorac (QNC) is important. In this work, a novel Ndopedcarbon support CoFe2O4/Fe0 hybrid catalyst (CFO/Fe@C) was in situ formed by a simple coprecipitationand calcination process. Fine intergrowth crystal CoFe2O4 and Fe0 were uniformly dispersedon the N-doped porous carbon that derived from the raw material Ethylene Diamine Tetraacetic Acid(EDTA), which also provided chelating effect to prevent the agglomeration of the metals. Interestingly,the Fe0 could only be formed with the presence of cobalt, possibly due to the increased reduction propertyresulted from the particle refinement. The as-formed Fe0 could not only activate the peroxymonosulfate(PMS) but also reduce the Co3+, resulting in a synergistic impact to remarkably enhance thedegradation performance. Besides, the N-doped porous carbon can also benefit the degradation of pollutantby strengthening the electron transfer. A good degradation efficiency of QNC was obtained in CFO/Fe@C-PMS system and most of the QNC had been degraded to carbon dioxide, water and other smallmolecular organisms. The removal rate remained over 70% after four reuses and the material could beeasily recovered from the solution due to the good magnetic properties. Therefore, the as-preparedCFO/Fe@C catalyst should be an ideal catalyst for the removal of organic pollutants.
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glyA Gene Knock-out in Escherichia coli Enhances L-serine Production without Glycine Addition
Ya Zhang,Pei Kang,Shuang Liu,Yujiao Zhao,Zhiwen Wang,Tao Chen 한국생물공학회 2017 Biotechnology and Bioprocess Engineering Vol.22 No.4
In E. coli, glyA encodes for serine hydroxymethyltransferase (SHMT), which converts L-serine to glycine. When engineering L-serine-producing strains, it is therefore favorable to inactivate glyA to prevent L-serine degradation. However, most glyA knockout strains exhibit slow cell growth because of the resulting lack of glycine and C1 units. To overcome this problem, we overexpressed the gcvTHP genes of the glycine cleavage system (GCV), to increase the C1 supply before glyA was knocked out. Subsequently, the kbl and tdh genes were overexpressed to provide additional glycine via the L-threonine degradation pathway, thus restoring normal cell growth independent of glycine addition. Finally, the plasmid pPK10 was introduced to overexpress pgk, serAΔ197, serC and serB, and the resulting strain E4G2 (pPK10) accumulated 266.3 mg/L of L-serine in a semi-defined medium without adding glycine, which was 3.18-fold higher than the production achieved by the control strain E3 (pPK10). This strategy can accordingly be applied to disrupt the L-serine degradation pathway in industrial production strains without causing negative side-effects, ultimately making L-serine production more efficient.
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Anqi Luo,Min Meng,Guanying Wang,Rui Han,Yujiao Zhang,Xin Jing,Lin Zhao,Shanzhi Gu,Xinhan Zhao 한국유방암학회 2020 Journal of breast cancer Vol.23 No.2
Purpose: Numerous studies have shown that the frequency of myeloid-derived suppressor cells (MDSCs) is associated with tumor progression, metastasis, and recurrence. Chemokine (C-C motif ) ligand 3 (CCL3) may be secreted by tumor cells and attract MDSCs into the tumor microenvironment. In the present study, we aimed to explore the molecular mechanisms whereby CCL3 is involved in the interaction of breast cancer cells and MDSCs. Methods: The expression of CCL3 and its receptors was investigated using real-time polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay. The cell counting Kit-8, wound healing, and transwell assays were performed to study cell growth, migration, and invasion. Cell cycling, apoptosis, and the frequency of MDSCs were investigated through flow cytometry. Transwell assays were used for co-culture and chemotaxis detection. Markers of the epithelial-mesenchymal transition (EMT) were determined with western blotting. The role of CCL3 in vivo was studied via tumor xenograft experiments. Results: CCL3 promoted cell proliferation, migration, invasion, and cycling, and inhibited apoptosis of breast cancer cells in vitro. Blocking CCL3 in vivo inhibited tumor growth and metastases. The frequency of MDSCs in patients with breast cancer was higher than that in healthy donors. Additionally, MDSCs might be recruited by CCL3. Co-culture with MDSCs activated the phosphoinositide 3-kinase-protein kinase B-mammalian target of rapamycin (PI3K-Akt-mTOR) pathway and promoted the EMT in breast cancer cells, and their proliferation, migration, and invasion significantly increased. These changes were not observed when breast cancer cells with CCL3 knockdown were co-cultured with MDSCs. Conclusion: CCL3 promoted the growth of breast cancer cells, and MDSCs recruited by CCL3 interacted with these cells and then activated the PI3K-Akt-mTOR pathway, which led to EMT and promoted the migration and invasion of the cells.
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